Alzheimer disease: 100 years later
Almost 100 years since the first clinical report of a case of Alzheimer disease (AD), three early-onset and two late-onset AD genes have been identified. While rare mutations in the early-onset genes (amyloid precursor protein, and presenilins 1 and 2) lead to increased generation of specific forms...
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| Autores principales: | , |
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| Lenguaje: | English |
| Publicado: |
Sociedad Médica de Santiago
2001
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| Materias: | |
| Acceso en línea: | http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872001000500015 |
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| Sumario: | Almost 100 years since the first clinical report of a case of Alzheimer disease (AD), three early-onset and two late-onset AD genes have been identified. While rare mutations in the early-onset genes (amyloid precursor protein, and presenilins 1 and 2) lead to increased generation of specific forms of the amyloid ß protein (A,ß), common polymorphisms in the late-onset genes (apolipoprotein E and alpha²-macroglobulin) are thought to alter the clearance and degradation of A,ß in brain. Although definite proof for a direct link between altered A ß generation/clearance and neurodegeneration has not yet been attained, mechanism-based approaches for the therapeutic treatment of AD based on lowering levels of the potentially pathogenic Aß are currently underway. The recent discovery of the enzymes (secretases) responsible for generating Aß have paved the way for the development of such drugs and increase the prospects for successful therapeutic intervention to arrest AD neuropathogenesis (Rev Méd Chile 2001; 129: 569-75) |
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